Enhancement of disease response in an immunized host has been observed in several viral infections of infants and children. One of these, the dengue shock syndrome (DSS), common in Southeast Asia is usually accompanied by a secondary antibody response. It is also seen in primarily infected infants who are born under epidemiological circumstances suggesting that their mothers were dengue immune during the gestational period. Enhancement of dengue disease might, therefore, result from endogenous infection experience or be regulated by a passively transferred factor. Previous studies in this laboratory suggest that enhanced dengue disease may result from an enhanced infection. Experimentally infected monkeys circulate more virus during a secondary than a primary infection. Peripheral leukocyte cultures from immune monkeys or humans support dengue infection readily, while cultures from normal monkeys or humans do not. Shock in dengue occurs when intracellular infection is eliminated, virus isolations from fatal cases are rare. Epidemiologic data for the sudden infant death syndrome (SIDS) suggest respiratory tract viral infection is frequently an antecedent event. We suggest that the effector mechanisms in primary infection dengue shock syndrome and SIDS may be the same, although the anatomical target organ differs. This study proposes to investigate two hypotheses: 1) that information for enhanced infection can be transmitted passively to cultured leukocytes or 2) that infection enhancement in the infant is the result of an infection of the mother during gestation. The dengue model will be used to study these questions. Methodologies will include conventional virus assay, leukocyte culture techniques, and immunochemical methods. Infection enhancing factor will be sought in serum, cord blood, colostrum, in sonicated leukocyte extract or in fragmented or whole leukocytes from dengue immune individuals. Dengue susceptible pregnant cynomologous monkeys will be infected with a dengue virus and leukocyte cultures from their progeny tested for infection enhancement.